Chronic ethanol intoxication during pregnancy causes fetal growth retardation in man and lower animals. A major concern in animal models of this condition is the control of nutrition. However potentially important dynamics are overlooked when nutritional variables are minimized. Studies on rats indicate that a single mild dose of ethanol, which has little effect on fetuses from well-fed dams, causes growth retardation when given to dams made acutely deficient in zinc. This 2-factor interaction is insidious; a brief period of subtle dietary deficiency creates a high-risk "window", within which acute maternal intoxication becauses dangerous to the fetus. The 2-factor model is used to examine the consequences of prenatal treatment on postnatal development in rats. The first phase of research determines if critical periods exist during which brief, interactive treatments are particularly harmful to the offspring. Litters treated at different gestational ages are compared for failure to thrive and delays in developmental milestones; neural sequelae of critical periods are sought. In the second phase treatments are timed to coincide with neurogenesis in the hippocampal region. Effects on the morphometry, morphology and function of this brain region are assessed using neuroanatomic and behavioral methods. The hippocampal region has been implicated in infantile neuropathology; this phase explores possible teratologic bases of such syndromes. Two-factor (interactive) teratology is viewed as more representative of the human environment than models varying only a single factor. The ultimate goal of the research is to determine nervous system reactions which may not be accompanied by gross malformations, but may nonetheless compromise postnatal development.